Abstract
Plasma extracellular vesicles (EVs) containing various molecules, including cytokines, can reflect the intracellular condition and participate in cell-to-cell signaling, thus emerging as biomarkers for Parkinson’s disease (PD). Inflammation may be a crucial risk factor for PD development and progression. The present study investigated the role of plasma EV cytokines as the biomarkers of PD. This cross-sectional study recruited 113 patients with PD, with mild to moderate stage disease, and 48 controls. Plasma EVs were isolated, and the levels of cytokines, including pro-interleukin (IL)-1β, IL-6, IL-10, tumor necrosis factor (TNF)-α, and transforming growth factor (TGF)-β1, were evaluated. Patients with PD had significantly increased plasma EV pro-IL-1β and TNF-α levels compared with controls after adjustment for age and sex. Despite the lack of a significant association between plasma EV cytokines and motor symptom severity in patients with PD, cognitive dysfunction severity, assessed using the Mini-Mental State Examination (MMSE) and Montreal Cognitive Assessment, was significantly associated with plasma EV pro-IL-1β, IL-6, IL-10, and TNF-α levels. This association was PD specific and not found in controls. Furthermore, patients with PD cognitive deficit (MMSE < 26) exhibited a distinguished EV cytokine profile compared to those without cognitive deficit. The findings support the concept of inflammatory pathogenesis in the development and progression of PD and indicate that plasma EV cytokines may serve as PD biomarkers in future.
Highlights
Parkinson’s disease (PD) is the second most common neurodegenerative disease [1], and its prevalence is expected to increase with the aging of society [2]
The results of the present study demonstrated that the levels of plasma extracellular vesicles (EVs) proinflammatory cytokines pro-IL-1β and tumor necrosis factor (TNF)-α were elevated in patients with PD compared with controls after adjustment for age and sex
The plasma EV cytokine profile was significantly associated with cognitive function in patients with PD but not in controls
Summary
Parkinson’s disease (PD) is the second most common neurodegenerative disease [1], and its prevalence is expected to increase with the aging of society [2]. Local inflammation of the brain (neuroinflammation) is a crucial environmental stress for the loss of dopaminergic neurons in PD. After the uptake of excessive α-synuclein from dopaminergic neurons, microglial cells activate and release proinflammatory cytokines, triggering inflammatory stress, which may induce neuronal apoptosis [7]. Systemic inflammation contributes to neuroinflammation; epidemiological studies have indicated a strong association between inflammatory bowel diseases and PD [8] and demonstrated the protective effect of nonsteroidal anti-inflammatory drugs on PD [9]. The concept of gut–brain axis supports the role of systemic inflammation in PD. Gut dysbiosis causes leaky gut syndrome, which allows proinflammatory lipopolysaccharides (LPSs) to enter the circulation and induce inflammation in the peripheral nervous system and brain simultaneously [10]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
